METHODOLOGY: This randomised, blinded end-point, placebo-controlled clinical trial with a parallel design involved 36 healthy male subjects who took either an oral placebo or TRE at doses of 80, 160 or 320 mg daily for 2 mo. Baseline and end-of-treatment measurements of vitamin E concentration, arterial compliance [assessed by aortic femoral pulse wave velocity (PWV) and augmentation index (AI)], ASBP, plasma TAS, serum TC and LDL-C were taken.
RESULTS: Baseline tocotrienol isomer concentrations were low and not detectable in some subjects. Upon supplementation, all TRE-treated groups showed significant difference from placebo for their change in alpha, gamma and delta tocotrienol concentrations from baseline to end of treatment. There was a linear dose and blood level relationship for all the isomers. There was no significant difference between groups for their change in PWV, AI, plasma TAS, ASBP, TC or LDL-C from baseline to end of treatment. Groups 160 mg (p = 0.024) and 320 mg (p = 0.049) showed significant reductions in their ASBP. Group 320 mg showed a significant 9.2% improvement in TAS.
CONCLUSION: TRE at doses up to 320 mg daily were well tolerated. Treatment significantly increased alpha, delta, and gamma tocotrienol concentrations but did not significantly affect arterial compliance, plasma TAS, serum TC or LDL-C levels in normal subjects.
METHODS: All patients with traumatic brain injury (mild, moderate, and severe) who were admitted to Queen Elizabeth Hospital from November 1, 2017, to January 31, 2019, were prospectively analyzed through a data collection sheet. The discriminatory power of the models was assessed as area under the receiver operating characteristic curve and calibration was assessed using the Hosmer-Lemeshow (H-L) goodness-of-fit test and Cox calibration regression analysis.
RESULTS: We analyzed 281 patients with significant TBI treated in a single neurosurgical center in Malaysia over a 2-year period. The overall observed 14-day mortality was 9.6%, a 6-month unfavorable outcome of 23.5%, and a 6-month mortality of 13.2%. Overall, both the CRASH and IMPACT models showed good discrimination with AUCs ranging from 0.88 to 0.94 and both models calibrating satisfactorily H-L GoF P>0.05 and calibration slopes >1.0 although IMPACT seemed to be slightly more superior compared to the CRASH model.
CONCLUSIONS: The CRASH and IMPACT prognostic models displayed satisfactory overall performance in our cohort of TBI patients, but further investigations on factors contributing to TBI outcomes and continuous updating on both models remain crucial.